The hypothesis that triglyceride-rich lipoproteins play a primary role in the development of arterial lesions will be tested in experimental animals. The hypothesis states that chylomicrons and very low density lipoproteins in plasma are adsorbed at arterial surfaces and are there degraded to cholesterol-rich remnants by the action of lipoprotein lipase. The remnants are subsequently transported into the intimal layer. Arterial lipoprotein lipase will be characterized and localized. The role of acid mucopolysaccharides in the adsorption of lipoproteins to the artery and in the activation of the lipase will be studied. Uptake of lipids and intact lipoproteins will be studied in intact animals as well as in perfused arteries and arterial strips. The role of phospholipids, both administered parenterally and biosynthesized in the artery, in the dissolution of plaques will be investigated. Model systems of isolated liver and spleen macrophages will also be used.